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Text
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URL Address
<a href="http://doi.org/10.1152/ajpendo.00327.2009" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpendo.00327.2009</a>
Pages
E1147–1153
Issue
5
Volume
297
Dublin Core
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Title
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Impact of type 1 diabetes on cardiac fibroblast activation: enhanced cell cycle progression and reduced myofibroblast content in diabetic myocardium.
Publisher
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American journal of physiology. Endocrinology and metabolism
Date
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2009
2009-11
Subject
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Animals; Blood Glucose/metabolism; Blotting; Body Weight/physiology; Cell Cycle Proteins/biosynthesis; Cell Cycle/*physiology; Cell Differentiation/physiology; Cell Proliferation; Cell Separation; Diabetes Mellitus; Echocardiography; Experimental/pathology; Fibroblasts/*physiology; Male; Microarray Analysis; Myocardium/cytology/*pathology; Myofibroblasts/*physiology; Phenotype; Rats; RNA/biosynthesis/isolation & purification; Signal Transduction/physiology; Sprague-Dawley; Type 1/diagnostic imaging/*pathology; Western
Creator
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Shamhart Patricia E; Luther Daniel J; Hodson Ben R; Koshy John C; Ohanyan Vahagn; Meszaros J Gary
Description
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Diabetic patients are prone to developing myocardial fibrosis and suffer from decreased wound healing capabilities. The purpose of this study was to determine whether diabetes alters cardiac fibroblast activity in the myocardium in a 6-wk streptozotocin-induced type 1 diabetic model. In vivo echocardiography indicated significant dilation of the left ventricle (LV) in the diabetic animals, while cardiac function was comparable to that in the normal group. We isolated cardiac fibroblasts from diabetic and control hearts and observed increased proliferation of the diabetic fibroblasts. Microarray analysis using mRNA collected from whole LVs revealed downregulation of known inhibitors of proliferation, p53 and p21, in the diabetic group, consistent with our proliferation data. Western blot analysis confirmed a reduction in p53 protein expression in the diabetic hearts compared with control. We explored the potential signaling underlying the downregulation of these cell cycle mediators and determined that activated Akt, a signal that inhibits p53, was elevated in the diabetic group. Surprisingly, the hearts from the diabetic group contained lower levels of the myofibroblast marker alpha-smooth muscle actin (alpha-SMA) and higher levels of desmin and platelet endothelial cell adhesion molecule (PECAM). The isolated fibroblasts from the diabetic group also contained significantly less alpha-SMA. These data suggest that early-stage diabetic hearts contain highly proliferative fibroblasts, which predisposes the diabetic myocardium to fibrosis, but have fewer myofibroblasts, which may compromise wound healing.
Identifier
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<a href="http://doi.org/10.1152/ajpendo.00327.2009" target="_blank" rel="noreferrer noopener">10.1152/ajpendo.00327.2009</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2009
American journal of physiology. Endocrinology and metabolism
Animals
Blood Glucose/metabolism
Blotting
Body Weight/physiology
Cell Cycle Proteins/biosynthesis
Cell Cycle/*physiology
Cell Differentiation/physiology
Cell Proliferation
Cell Separation
Department of Integrative Medical Sciences
Diabetes Mellitus
Echocardiography
Experimental/pathology
Fibroblasts/*physiology
Hodson Ben R
Koshy John C
Luther Daniel J
Male
Meszaros J Gary
Microarray Analysis
Myocardium/cytology/*pathology
Myofibroblasts/*physiology
NEOMED College of Medicine
Ohanyan Vahagn
Phenotype
Rats
RNA/biosynthesis/isolation & purification
Shamhart Patricia E
Signal Transduction/physiology
Sprague-Dawley
Type 1/diagnostic imaging/*pathology
Western